Fibrosis of organs occurs in such a manner that extracellular matrix is excessively accumulated in the organs through invasion or injury of organs due to some cause. When the degree of damage of organs due to invasion or injury is slight, cicatrix does not remain and the organs return to normal. However, when the degree of damage of the organs due to invasion or injury is severe or sustained, fibrosis of the cicatrix gives impairment of its inherent function. Further, it induces new fibrosis and generates a vicious cycle of fibrosis, finally, dysfunction of organs occurs.
As a disease caused by fibrosis of organs, interstitial pneumonia (pulmonary fibrosis), etc. have been known. Interstitial pneumonia is a disease where inflammation happens in alveolar wall due to some causes; fibroblasts proliferate in interstitial tissues; the lung is sclerosed by an excessive sedimentation of collagen fibers; gas exchange is disturbed; and, finally, respiratory failure occurs. After onset of the disease, the patient dies within three to five years in average. The detailed mechanism of pathogenesis of interstitial pneumonia has not been clarified yet and no established treating method has been available yet as well.
It has recently been reported that, in interstitial pneumonia model mice induced by bleomycin, ONO-1301 which is a prostaglandin I2 (hereinafter, referred to as “PGI2”) receptor agonist has a inhibitive effect for interstitial pneumonia (see, for example, Non-Patent Document 1).
The present heterocyclic derivative (1) or a pharmaceutically acceptable salt thereof has already been reported to be useful for the treatment of pulmonary hypertension and obstructive arteriosclerosis as a PGI2 receptor agonist (see, for example, Patent Document 1).    Patent Document 1: Pamphlet of International Publication WO 02/088084    Non-Patent Document 1: Am J Physiol Lung Cell Mol Physiol 290: L59-L65, 2006